Review



hut78 cutaneous t cell lymphoma cell line  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 96

    Structured Review

    ATCC hut78 cutaneous t cell lymphoma cell line
    Hut78 Cutaneous T Cell Lymphoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 584 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/HuT+78/pmc13006415-480-20-27
    Average 96 stars, based on 584 article reviews
    hut78 cutaneous t cell lymphoma cell line - by Bioz Stars, 2026-10
    96/100 stars

    Images

    Related Articles

    Olfactory:

    Article Title: Olfactory Receptors as Tumor Suppressors in Cutaneous T-Cell Lymphoma via p38γ Pathway Modulation
    Article Snippet: In line with these findings, our current study uncovered the role of p38γ in CTCL cells and elucidated its molecular dynamics that impinge on ORs within the framework of the TCR signaling pathway via two small molecules CSH71 and CSH18 that targeting p38γ’s lipid binding site. .. Previously, we showed that CSH71 (250 nM) strongly upregulates the Olfactory Transduction pathway in Hut78 cells (CD4+, Sézary syndrome, ATCC) via RNA microarray4. ..

    Article Title: Olfactory receptors as tumor suppressors in cutaneous T-cell lymphoma via p38γ pathway modulation
    Article Snippet: .. Previously, we showed that CSH71 (250 nM) strongly upregulates the olfactory transduction pathway in Hut78 cells (CD4 + , SS; American Type Culture Collection) via RNA microarray. ..

    Transduction:

    Article Title: Olfactory Receptors as Tumor Suppressors in Cutaneous T-Cell Lymphoma via p38γ Pathway Modulation
    Article Snippet: In line with these findings, our current study uncovered the role of p38γ in CTCL cells and elucidated its molecular dynamics that impinge on ORs within the framework of the TCR signaling pathway via two small molecules CSH71 and CSH18 that targeting p38γ’s lipid binding site. .. Previously, we showed that CSH71 (250 nM) strongly upregulates the Olfactory Transduction pathway in Hut78 cells (CD4+, Sézary syndrome, ATCC) via RNA microarray4. ..

    Article Title: Olfactory receptors as tumor suppressors in cutaneous T-cell lymphoma via p38γ pathway modulation
    Article Snippet: .. Previously, we showed that CSH71 (250 nM) strongly upregulates the olfactory transduction pathway in Hut78 cells (CD4 + , SS; American Type Culture Collection) via RNA microarray. ..

    Microarray:

    Article Title: Olfactory receptors as tumor suppressors in cutaneous T-cell lymphoma via p38γ pathway modulation
    Article Snippet: .. Previously, we showed that CSH71 (250 nM) strongly upregulates the olfactory transduction pathway in Hut78 cells (CD4 + , SS; American Type Culture Collection) via RNA microarray. ..

    Cell Binding Assay:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Transfection:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Expressing:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Plasmid Preparation:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Selection:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Cell Culture:

    Article Title: Reprogramming of PD-1+ M2-like tumor-associated macrophages with anti-PD-L1 and lenalidomide in cutaneous T cell lymphoma.
    Article Snippet: .. Cell culture MyLa and Hut78 cells were purchased from American Type Culture Collection (ATCC) and cultured in RPMI 1640 (Corning, catalog 10-040-cv) or IMDM (Gibco, catalog 12440053), supplemented with 10% FBS (Corning, catalog 35-010-CV), 100 IU/mL penicillin and 100 μg/mL (Gibco, catalog 15140122) streptomycin in a humidified, 5% CO2 incubator at 37°C. ..

    Article Title: Reprogramming of PD-1 + M2-like tumor-associated macrophages with anti–PD-L1 and lenalidomide in cutaneous T cell lymphoma
    Article Snippet: .. MyLa and Hut78 cells were purchased from American Type Culture Collection (ATCC) and cultured in RPMI 1640 (Corning, catalog 10-040-cv) or IMDM (Gibco, catalog 12440053), supplemented with 10% FBS (Corning, catalog 35-010-CV), 100 IU/mL penicillin and 100 μg/mL (Gibco, catalog 15140122) streptomycin in a humidified, 5% CO 2 incubator at 37°C. ..

    Generated:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.

    Stable Transfection:

    Article Title: BGB-A445, a novel non-ligand-blocking agonistic anti-OX40 antibody, exhibits superior immune activation and antitumor effects in preclinical models.
    Article Snippet: OX40 is a costimulatory receptor that is expressed primarily on activated CD4+, CD8+, and regulatory T cells.. The ligation of OX40 to its sole ligand OX40L potentiates T cell expansion, differentiation, and activation and also promotes dendritic cells to mature to enhance their cytokine production.. Therefore, the use of agonistic anti-OX40 antibodies for cancer immunotherapy has gained great interest.



    Similar Products

    96
    ATCC hut78 cutaneous t cell lymphoma cell line
    Hut78 Cutaneous T Cell Lymphoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/HuT+78/pmc13006415-480-20-27
    Average 96 stars, based on 1 article reviews
    hut78 cutaneous t cell lymphoma cell line - by Bioz Stars, 2026-10
    96/100 stars
      Buy from Supplier

    99
    InvivoGen hut78 cells
    HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using <t>HuT78</t> cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.
    Hut78 Cells, supplied by InvivoGen, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/Puromycin/pmc13158664-72-6-20
    Average 99 stars, based on 1 article reviews
    hut78 cells - by Bioz Stars, 2026-10
    99/100 stars
      Buy from Supplier

    96
    ATCC cell lines hut78 atcc tib
    HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using <t>HuT78</t> cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.
    Cell Lines Hut78 Atcc Tib, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/HuT+78/pm41709452-499-158-161
    Average 96 stars, based on 1 article reviews
    cell lines hut78 atcc tib - by Bioz Stars, 2026-10
    96/100 stars
      Buy from Supplier

    96
    ATCC hut78 t lymphocyte cell lines
    HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using <t>HuT78</t> cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.
    Hut78 T Lymphocyte Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/HuT+78/pmc12881303-10-3-17
    Average 96 stars, based on 1 article reviews
    hut78 t lymphocyte cell lines - by Bioz Stars, 2026-10
    96/100 stars
      Buy from Supplier

    86
    Charles River Laboratories hut78 cells
    HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using <t>HuT78</t> cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.
    Hut78 Cells, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/cells+hut78/10__3390_slash_ijms27031408-199-0-18
    Average 86 stars, based on 1 article reviews
    hut78 cells - by Bioz Stars, 2026-10
    86/100 stars
      Buy from Supplier

    86
    Bio-Tech Pharmacal Inc hut78 cells
    ENO1 is overexpressed in PTCL-NOS tissues and cell lines. (A) ENO1 expression in PTCL-NOS and NON (normal tissues) analyzed using TCGA data. (B) RT-qPCR detection of ENO1 mRNA levels in normal PBMCs and PTCL-NOS cell lines (Jurkat, Karpas299, <t>Hut78).</t> (C, E, G) Knockdown efficiency of shENO1 in Jurkat, Karpas299, and Hut78 cells confirmed by RT-qPCR. (D, F, H) Western blot validation of ENO1 protein downregulation in shRNA-transduced cells. * p < 0.050, *** p < .001 vs control. ENO1 = enolase, PBMC = peripheral blood mononuclear cell, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, RT-qPCR = reverse transcription quantitative polymerase chain reaction, TCGA = The Cancer Genome Atlas.
    Hut78 Cells, supplied by Bio-Tech Pharmacal Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/cells+hut78/pmc12829720-34-35-12
    Average 86 stars, based on 1 article reviews
    hut78 cells - by Bioz Stars, 2026-10
    86/100 stars
      Buy from Supplier

    99
    ATCC inc benchmark antibody okt3 abcam ab86883 jurkat cells atcc tib 152 hut78 cells atcc ecacc 880401901 molt 4 cells atcc crl
    ENO1 is overexpressed in PTCL-NOS tissues and cell lines. (A) ENO1 expression in PTCL-NOS and NON (normal tissues) analyzed using TCGA data. (B) RT-qPCR detection of ENO1 mRNA levels in normal PBMCs and PTCL-NOS cell lines (Jurkat, Karpas299, <t>Hut78).</t> (C, E, G) Knockdown efficiency of shENO1 in Jurkat, Karpas299, and Hut78 cells confirmed by RT-qPCR. (D, F, H) Western blot validation of ENO1 protein downregulation in shRNA-transduced cells. * p < 0.050, *** p < .001 vs control. ENO1 = enolase, PBMC = peripheral blood mononuclear cell, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, RT-qPCR = reverse transcription quantitative polymerase chain reaction, TCGA = The Cancer Genome Atlas.
    Inc Benchmark Antibody Okt3 Abcam Ab86883 Jurkat Cells Atcc Tib 152 Hut78 Cells Atcc Ecacc 880401901 Molt 4 Cells Atcc Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hut78+cells/Jurkat%2C+Clone+E6-1/us12486325-598-31-39
    Average 99 stars, based on 1 article reviews
    inc benchmark antibody okt3 abcam ab86883 jurkat cells atcc tib 152 hut78 cells atcc ecacc 880401901 molt 4 cells atcc crl - by Bioz Stars, 2026-10
    99/100 stars
      Buy from Supplier

    Image Search Results


    HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using HuT78 cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.

    Journal: Nucleic Acids Research

    Article Title: A viral noncoding RNA is a master regulator of gene expression that defines host cell identity and function

    doi: 10.1093/nar/gkag472

    Figure Lengend Snippet: HSUR1 reprograms host gene expression and promotes cell survival. ( A ) GO and KEGG pathway analyses showing selected categories significantly enriched among HSUR1 target mRNAs. ( B ) Flow cytometry of cj38637-WT and cj38637-ΔHSUR1 cells stained with Annexin V–Alexa Fluor 647 and propidium iodide; quantification from three independent experiments shown on the right. ( C ) Caspase-3/7 activity in WT and ΔHSUR1 cells measured by Caspase-Glo 3/7 assay after FasL treatment. ( D ) Same as in panel (C), using HuT78 cells transduced with lentiviral vectors expressing GFP (control) or HSUR1 and treated with vehicle or FasL. ( E ) Volcano plot of differentially expressed transcripts in cj38637-ΔHSUR1 versus cj38637-WT cells. Y axis shows two different scales (separated by a break), with significant adjusted P -values shown above the dashed lines. ( F ) Summary of changes in intron retention and alternative splice site usage. ( G ) Summary of differentially spliced cassette exons. NCE, noncoding transcript exon; 5′UTR, 5′ untranslated region exon; FCE, first coding exon; FS-CE, frameshifting internal coding exon; non-FS-CE, non-frameshifting internal coding exon; LCE, last coding exon. *** P < .001, **** P < .0001.

    Article Snippet: Stably transduced firefly- and Renilla -luciferase-expressing HuT78 cells (see below) were grown in complete medium plus 8 μg/ml of puromycin (InvivoGen) and 10 μg/ml of blasticidin (InvivoGen), whereas stably transduced HuT78 and HeLa cells expressing WT or mutant versions of HSUR1 were grown in complete medium plus 10 or 8 μg/ml of puromycin, respectively.

    Techniques: Gene Expression, Flow Cytometry, Staining, Activity Assay, Caspase-Glo Assay, Transduction, Expressing, Control

    Dual role of the HSUR1 ARE in RNA stability and target repression. ( A ) Northern blot showing HSUR1 levels in HeLa-H1 cells transfected with control siRNA or siRNAs targeting KHSRP, HuR, or hnRNP D. U1 serves as a loading control. Quantification of three independent experiments is shown on the right; U1 snRNA signal was used for normalization. ( B ) Sequence of the HSUR1 5′ end and miR-142-3p showing mutations disrupting the first (m1), second (m2), or third (m3) AUUUA motif. ( C ) Reporter assay using HuT78 cells expressing the luciferase-PPFIA1 3′UTR reporter and co-transfected with mCherry/V5-ZFP36L2 and WT or mutant HSUR1 constructs as in panel (B). ( D ) Co-immunoprecipitation of miRNAs with αSm antibodies from HeLa-H1, HeLa-H1m142, and HeLa-H1-AREm1–m3 cells transfected with miR-142-3p. Northern blot probed for miRNAs, HSUR1, and U1 (immunoprecipitation control). Input, 5%; αSm IP, 100%. ( E ) Enrichment of HSUR1 target and control mRNAs in KHSRP immunoprecipitates from cj38637-WT and cj38637-ΔHSUR1 cells. Western blots on the right show IP efficiency using normal rabbit serum control and αKHSRP antibodies (E2E2U). Input, 5%; IP, 100%. ( F ) Same as in panel (E) using V5 immunoprecipitates from HeLa cells co-transfected with mCherry/V5-ZFP36L2 and either control or miR-142-3p.

    Journal: Nucleic Acids Research

    Article Title: A viral noncoding RNA is a master regulator of gene expression that defines host cell identity and function

    doi: 10.1093/nar/gkag472

    Figure Lengend Snippet: Dual role of the HSUR1 ARE in RNA stability and target repression. ( A ) Northern blot showing HSUR1 levels in HeLa-H1 cells transfected with control siRNA or siRNAs targeting KHSRP, HuR, or hnRNP D. U1 serves as a loading control. Quantification of three independent experiments is shown on the right; U1 snRNA signal was used for normalization. ( B ) Sequence of the HSUR1 5′ end and miR-142-3p showing mutations disrupting the first (m1), second (m2), or third (m3) AUUUA motif. ( C ) Reporter assay using HuT78 cells expressing the luciferase-PPFIA1 3′UTR reporter and co-transfected with mCherry/V5-ZFP36L2 and WT or mutant HSUR1 constructs as in panel (B). ( D ) Co-immunoprecipitation of miRNAs with αSm antibodies from HeLa-H1, HeLa-H1m142, and HeLa-H1-AREm1–m3 cells transfected with miR-142-3p. Northern blot probed for miRNAs, HSUR1, and U1 (immunoprecipitation control). Input, 5%; αSm IP, 100%. ( E ) Enrichment of HSUR1 target and control mRNAs in KHSRP immunoprecipitates from cj38637-WT and cj38637-ΔHSUR1 cells. Western blots on the right show IP efficiency using normal rabbit serum control and αKHSRP antibodies (E2E2U). Input, 5%; IP, 100%. ( F ) Same as in panel (E) using V5 immunoprecipitates from HeLa cells co-transfected with mCherry/V5-ZFP36L2 and either control or miR-142-3p.

    Article Snippet: Stably transduced firefly- and Renilla -luciferase-expressing HuT78 cells (see below) were grown in complete medium plus 8 μg/ml of puromycin (InvivoGen) and 10 μg/ml of blasticidin (InvivoGen), whereas stably transduced HuT78 and HeLa cells expressing WT or mutant versions of HSUR1 were grown in complete medium plus 10 or 8 μg/ml of puromycin, respectively.

    Techniques: Northern Blot, Transfection, Control, Sequencing, Reporter Assay, Expressing, Luciferase, Mutagenesis, Construct, Immunoprecipitation, Western Blot

    HSUR1 determines cell identity and function. ( A ) Western blot of representative HSUR1 target proteins in cj38637-WT and cj38637-ΔHSUR1 cells; cofilin serves as a loading control. ( B ) IFN-γ production in cj38637-WT and cj38637-ΔHSUR1 cells detected by western blot after PMA/ionomycin stimulation in the presence of brefeldin A and monensin; quantification of three replicates shown at right. HDAC1 provides a loading control. ( C ) Predicted composition of resting (R) and active (A) immune cell types inferred from gene expression using CIBERSORTx. T-reg, regulatory T cell; γδ-T, gamma-delta T cell; Tfh, T follicular helper cell; DC, dendritic cell; MΦ, macrophage; NK, natural killer cell. ( D ) NK-like cytotoxic activity of WT and ΔHSUR1 cells toward MOLT-4 target cells measured by CytoTox-Glo assay. ( E ) Flow cytometry analysis of cj38637-WT and cj38637-ΔHSUR1 cells for the indicated surface markers. ( F ) Same as in panel (E) for the indicated markers in HuT78 cells (Control) or same cells transduced with a lentiviral vector expressing HSUR1. * P < .05, ** P < 0.01, **** P < .0001.

    Journal: Nucleic Acids Research

    Article Title: A viral noncoding RNA is a master regulator of gene expression that defines host cell identity and function

    doi: 10.1093/nar/gkag472

    Figure Lengend Snippet: HSUR1 determines cell identity and function. ( A ) Western blot of representative HSUR1 target proteins in cj38637-WT and cj38637-ΔHSUR1 cells; cofilin serves as a loading control. ( B ) IFN-γ production in cj38637-WT and cj38637-ΔHSUR1 cells detected by western blot after PMA/ionomycin stimulation in the presence of brefeldin A and monensin; quantification of three replicates shown at right. HDAC1 provides a loading control. ( C ) Predicted composition of resting (R) and active (A) immune cell types inferred from gene expression using CIBERSORTx. T-reg, regulatory T cell; γδ-T, gamma-delta T cell; Tfh, T follicular helper cell; DC, dendritic cell; MΦ, macrophage; NK, natural killer cell. ( D ) NK-like cytotoxic activity of WT and ΔHSUR1 cells toward MOLT-4 target cells measured by CytoTox-Glo assay. ( E ) Flow cytometry analysis of cj38637-WT and cj38637-ΔHSUR1 cells for the indicated surface markers. ( F ) Same as in panel (E) for the indicated markers in HuT78 cells (Control) or same cells transduced with a lentiviral vector expressing HSUR1. * P < .05, ** P < 0.01, **** P < .0001.

    Article Snippet: Stably transduced firefly- and Renilla -luciferase-expressing HuT78 cells (see below) were grown in complete medium plus 8 μg/ml of puromycin (InvivoGen) and 10 μg/ml of blasticidin (InvivoGen), whereas stably transduced HuT78 and HeLa cells expressing WT or mutant versions of HSUR1 were grown in complete medium plus 10 or 8 μg/ml of puromycin, respectively.

    Techniques: Western Blot, Control, Gene Expression, Activity Assay, Glo Assay, Flow Cytometry, Transduction, Plasmid Preparation, Expressing

    HSUR1 regulates target mRNAs through sequences defined by iRICC-seq. ( A ) Schematic of constructs used for stable expression of luciferase reporters and transient expression of HSUR1. Renilla luciferase was expressed from the spleen focus-forming virus promoter, and firefly luciferase from the thymidine kinase (TK) promoter, either without a 3′UTR (Control) or fused to partial 3′UTRs of HSUR1 target mRNAs. ( B ) Luciferase assays validating HSUR1 binding sites. Normalized luciferase levels in FACS-sorted, GFP-positive HuT78 cells stably expressing either control or 3′UTR-containing luciferase reporters after transient transfection with the indicated plasmids. The sizes of 3′UTR fragments (in base pairs) are indicated between parentheses. ( C ) Same as in panel (B) but using reporters containing individual HSUR1 binding sites. ( D-E ) Same as in panel (C) for HNRNPA2B1 (A2B1)-BS2mut (D) and JARID2-BS2mut (E) reporters. * P < .05; ** P < .01; *** P < .001.

    Journal: Nucleic Acids Research

    Article Title: A viral noncoding RNA is a master regulator of gene expression that defines host cell identity and function

    doi: 10.1093/nar/gkag472

    Figure Lengend Snippet: HSUR1 regulates target mRNAs through sequences defined by iRICC-seq. ( A ) Schematic of constructs used for stable expression of luciferase reporters and transient expression of HSUR1. Renilla luciferase was expressed from the spleen focus-forming virus promoter, and firefly luciferase from the thymidine kinase (TK) promoter, either without a 3′UTR (Control) or fused to partial 3′UTRs of HSUR1 target mRNAs. ( B ) Luciferase assays validating HSUR1 binding sites. Normalized luciferase levels in FACS-sorted, GFP-positive HuT78 cells stably expressing either control or 3′UTR-containing luciferase reporters after transient transfection with the indicated plasmids. The sizes of 3′UTR fragments (in base pairs) are indicated between parentheses. ( C ) Same as in panel (B) but using reporters containing individual HSUR1 binding sites. ( D-E ) Same as in panel (C) for HNRNPA2B1 (A2B1)-BS2mut (D) and JARID2-BS2mut (E) reporters. * P < .05; ** P < .01; *** P < .001.

    Article Snippet: Stably transduced firefly- and Renilla -luciferase-expressing HuT78 cells (see below) were grown in complete medium plus 8 μg/ml of puromycin (InvivoGen) and 10 μg/ml of blasticidin (InvivoGen), whereas stably transduced HuT78 and HeLa cells expressing WT or mutant versions of HSUR1 were grown in complete medium plus 10 or 8 μg/ml of puromycin, respectively.

    Techniques: Construct, Expressing, Luciferase, Virus, Control, Binding Assay, Stable Transfection, Transfection

    HSUR1 represses target mRNAs through their 3′UTRs. ( A ) Quantitative real-time polymerase chain reaction (qRT-PCR) analysis of representative HSUR1 target mRNAs bound only at the 3′UTR (ADAR, HNRNPA2B1, FOXN3, PIP4K2B, UBA2, ILRUN, and JARID2) and control mRNAs (RABEP1, ECPAS, and GAA) in cj38637-WT and cj38637-ΔHSUR1 cells. ( B ) Western blot of HSUR1 targets in cj38637-WT and cj38637-ΔHSUR1 cells. Cofilin provides a loading control. ( C ) As in panel (A) in cj319-WT cells transiently transfected with control or HSUR1 ASO. ( D ) As in panel (A) in HuT78 cells sorted by FACS for GFP after transient transfection with either a plasmid expressing GFP and the U1 snRNA promoter (Control) or a plasmid expressing GFP and HSUR1 under the U1 promoter (HSUR1). * P < .05; ** P < .01; *** P < .001; **** P < .0001.

    Journal: Nucleic Acids Research

    Article Title: A viral noncoding RNA is a master regulator of gene expression that defines host cell identity and function

    doi: 10.1093/nar/gkag472

    Figure Lengend Snippet: HSUR1 represses target mRNAs through their 3′UTRs. ( A ) Quantitative real-time polymerase chain reaction (qRT-PCR) analysis of representative HSUR1 target mRNAs bound only at the 3′UTR (ADAR, HNRNPA2B1, FOXN3, PIP4K2B, UBA2, ILRUN, and JARID2) and control mRNAs (RABEP1, ECPAS, and GAA) in cj38637-WT and cj38637-ΔHSUR1 cells. ( B ) Western blot of HSUR1 targets in cj38637-WT and cj38637-ΔHSUR1 cells. Cofilin provides a loading control. ( C ) As in panel (A) in cj319-WT cells transiently transfected with control or HSUR1 ASO. ( D ) As in panel (A) in HuT78 cells sorted by FACS for GFP after transient transfection with either a plasmid expressing GFP and the U1 snRNA promoter (Control) or a plasmid expressing GFP and HSUR1 under the U1 promoter (HSUR1). * P < .05; ** P < .01; *** P < .001; **** P < .0001.

    Article Snippet: Stably transduced firefly- and Renilla -luciferase-expressing HuT78 cells (see below) were grown in complete medium plus 8 μg/ml of puromycin (InvivoGen) and 10 μg/ml of blasticidin (InvivoGen), whereas stably transduced HuT78 and HeLa cells expressing WT or mutant versions of HSUR1 were grown in complete medium plus 10 or 8 μg/ml of puromycin, respectively.

    Techniques: Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Control, Western Blot, Transfection, Plasmid Preparation, Expressing

    ENO1 is overexpressed in PTCL-NOS tissues and cell lines. (A) ENO1 expression in PTCL-NOS and NON (normal tissues) analyzed using TCGA data. (B) RT-qPCR detection of ENO1 mRNA levels in normal PBMCs and PTCL-NOS cell lines (Jurkat, Karpas299, Hut78). (C, E, G) Knockdown efficiency of shENO1 in Jurkat, Karpas299, and Hut78 cells confirmed by RT-qPCR. (D, F, H) Western blot validation of ENO1 protein downregulation in shRNA-transduced cells. * p < 0.050, *** p < .001 vs control. ENO1 = enolase, PBMC = peripheral blood mononuclear cell, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, RT-qPCR = reverse transcription quantitative polymerase chain reaction, TCGA = The Cancer Genome Atlas.

    Journal: Blood Science

    Article Title: ENO1 inhibition synergizes with chidamide to induce ferroptosis in PTCL-NOS through metabolic remodeling

    doi: 10.1097/BS9.0000000000000272

    Figure Lengend Snippet: ENO1 is overexpressed in PTCL-NOS tissues and cell lines. (A) ENO1 expression in PTCL-NOS and NON (normal tissues) analyzed using TCGA data. (B) RT-qPCR detection of ENO1 mRNA levels in normal PBMCs and PTCL-NOS cell lines (Jurkat, Karpas299, Hut78). (C, E, G) Knockdown efficiency of shENO1 in Jurkat, Karpas299, and Hut78 cells confirmed by RT-qPCR. (D, F, H) Western blot validation of ENO1 protein downregulation in shRNA-transduced cells. * p < 0.050, *** p < .001 vs control. ENO1 = enolase, PBMC = peripheral blood mononuclear cell, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, RT-qPCR = reverse transcription quantitative polymerase chain reaction, TCGA = The Cancer Genome Atlas.

    Article Snippet: The Karpas299, Hut78, and Jurkat cell lines were purchased from Nanjing Kexing Bio-Tech Co., Ltd. Karpas299 and Jurkat cells were cultured in medium supplemented with 10% fetal bovine serum (FBS) and 100 μg/mL penicillin/streptomycin, whereas Hut78 cells were cultured in medium supplemented with 20% FBS and 100 μg/mL penicillin/streptomycin.

    Techniques: Expressing, Quantitative RT-PCR, Knockdown, Western Blot, Biomarker Discovery, shRNA, Control, Reverse Transcription, Real-time Polymerase Chain Reaction

    Effects of ENO1 knockdown on proliferation, migration, and EMT in PTCL-NOS cells. (A–B) Cell proliferation in the Karpas299 and Jurkat cell lines detected by CCK-8 assay. (C) Karpas299 and Hut78 cell proliferation assessed by colony formation assay. (D) Migration of Karpas299 and Jurkat cells detected by Transwell assay (** p < 0.010, *** p < .001 compared with the control group). (E) Western blot analysis of N-cadherin and E-cadherin protein expression following ENO1 knockdown. ENO1 = enolase, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, EMT = epithelial-mesenchymal transition.

    Journal: Blood Science

    Article Title: ENO1 inhibition synergizes with chidamide to induce ferroptosis in PTCL-NOS through metabolic remodeling

    doi: 10.1097/BS9.0000000000000272

    Figure Lengend Snippet: Effects of ENO1 knockdown on proliferation, migration, and EMT in PTCL-NOS cells. (A–B) Cell proliferation in the Karpas299 and Jurkat cell lines detected by CCK-8 assay. (C) Karpas299 and Hut78 cell proliferation assessed by colony formation assay. (D) Migration of Karpas299 and Jurkat cells detected by Transwell assay (** p < 0.010, *** p < .001 compared with the control group). (E) Western blot analysis of N-cadherin and E-cadherin protein expression following ENO1 knockdown. ENO1 = enolase, PTCL-NOS = peripheral T cell lymphoma, not otherwise specified, EMT = epithelial-mesenchymal transition.

    Article Snippet: The Karpas299, Hut78, and Jurkat cell lines were purchased from Nanjing Kexing Bio-Tech Co., Ltd. Karpas299 and Jurkat cells were cultured in medium supplemented with 10% fetal bovine serum (FBS) and 100 μg/mL penicillin/streptomycin, whereas Hut78 cells were cultured in medium supplemented with 20% FBS and 100 μg/mL penicillin/streptomycin.

    Techniques: Knockdown, Migration, CCK-8 Assay, Colony Assay, Transwell Assay, Control, Western Blot, Expressing